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Pathology > Block 10 > Flashcards

Block 10 Flashcards

1
Q

What are the 5 cardinal signs

A 
Rubor
Calor
Dolor
Tumor
Functio laesa
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2
Q

Neutrophils are present in what inflammation

A

Acute

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3
Q

Where are neutrophils found

A

50% in circulation

50% in marginating pool

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4
Q

What is neutrophil distribution influenced by

A

Cytokines

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5
Q

What is the process of neutrophils adhesion

A
  1. IL-1 and TNF increas expression of selection
  2. Neutrophils weakly bin to selections and roll on surface
  3. Neutrophils express ligands for cellular adhesion molecules
  4. Neutrophils adhere firmly to ICAMS and VCAMS
  5. Neutrophils emigrate and migrate through tissues, phagocytize and kill what has been eaten
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6
Q

Where are a vast majority of mast cells found

A

Skin and lungs

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7
Q

What are chemical mediators of inflammation

A

Histamine
Serotonin
Kinins

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8
Q

What is histamine produced by

A

Basophils, platelets, and mast cells

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9
Q

What is release of histamine triggered by

A

IgE
Anaphylatoxins
IL-1

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10
Q

How is bradykinin made

A

Coag factor 7 converts prekallikrein to kallikrein

Which is then cleaved into bradykinin

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11
Q

What are the affects of bradykinin

A 
Vasodilation
Pain
Increased vascular permeability
Bronchoconstriction
Pain
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12
Q

What is made in the COX pathway

A

TXA2: made by platelets and causes vasoconstriction and platelet aggregation
Prostaglandin E2: causes pain and fever and vasodilation

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13
Q

What is made in the LOX pathway

A

Leukotrienes

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14
Q

What step in the arachidonic acid pathway is stopped by aspirin

A

COX (TXA2)

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15
Q

What are leukotrienes bad for

A

Asthma

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16
Q

What do IL1 and TNF do

A

Activate endothelial cell adhesion molecules

Initiate PGE2 synthesis in hypothalamus

Fever

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17
Q

What does IL6 act on

A

The liver to produce APR, ferritin, fibrinogen, CRP

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18
Q

What does IL-8 do

A

PMN chemotaxis

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19
Q

What are the 4 outcomes of acute inflammation

A

Complete resolution with regeneration

Complete resolution with scarring

Abscess formation

Transition into chronic inflammation

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20
Q

What are the causes of chronic infection

A

Persistent infections

Infections with recalcitrant organisms

Autoimmune disease

Response to foreign material

Response to malignant tumor

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21
Q

Where are macrophages circulating

A

In the blood

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22
Q

What are some macrophages

A 
Histiocytes (connective tissue)
Pulmonary alveolar macrophages (lung)
Kupffer (liver)
Osteoclasts (bone)
Microglia (brain)
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23
Q

What are modified into epithelioid cells in granluomas

A

Macrophages

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24
Q

What do eosinophils play a role in

A

Parasitic and allergic reactions

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25
Q

What s contained in eosinophils granules

A

Major basic protein, which is toxic to parasites

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26
Q

Basophils and masts release

A

Histamine

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27
Q

What is a granuloma

A

An epithelioid mass surrounded by lymphocytes

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28
Q

What is produced in necrosis

A

Exudate, pus that is filled with proteins and neutrophils

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29
Q

What are the 2 processes of necrosis

A
  1. Enzymatic digestion of the cell

2. Desaturation of proteins

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30
Q

What are the 4 types of necrosis

A

Coagulative
Liquefaction
Caseous
Fat

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31
Q

What is coagulative necrosis

A

Dues to ischemia or infarction

It is aseptic

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32
Q

Can regeneration occur in coagulative necrosis

A

It may if enough viable cells are present

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33
Q

What kind of necrosis is casused by ischemia is the brain

A

Liquefactive because there is very little structural framework in neural tissue

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34
Q

What is liquefactive necrosis

A

Leaves pus and fluid remains forms an abscess

Associated with bacterial or fungal infections

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35
Q

What is caseous necrosis

A

Most often observed in TB

Cheesy proteinaceous dead cell mass

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36
Q

What is fat necrosis

A

Death in adipose tissue
Small white lesions are formed

Due to trauma

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37
Q

What is apoptosis

A

Well organized cell death
Critical in fine tuning the retina and in fetal development

70% of ganglion cells die

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38
Q

What is Type 1 hypersensitivity

A

Anaphylactic

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39
Q

What is the 2 hypersensitivity

A

Cytotoxic

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40
Q

What is type 3 hypersensitivity

A

Immune complex

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41
Q

What is type 4 hypersensitivity

A

Delayed

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42
Q

What are early mediators of anaphylaxis

A

Histamine
Heparin
Eosinophils
Neutrophils chemotaxic factor (IL8)

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43
Q

What are the late mediators of anaphylaxis

A

Prostaglandins
Thromboxanes
Leukotrienes
SRS-A

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44
Q

Leukotrienes are _____ more potent than histamine

A

1000X

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45
Q

What does IL4 do

A

Drives IgM to IgE

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46
Q

What does IL5 do

A

Activate eosinophils

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47
Q

IL-13 does

A

Massive IgE production

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48
Q

What is the initial phase of type 1 driven by

A

Histamine

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49
Q

What is the last phase of Phase 1 driven by

A

Prostaglandins and leukotrienes

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50
Q

Leuoktrienes are _______X more potent than histamine

A

1000

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51
Q

What are some clinical manifestations of r Type 1 reaction

A 
Anaphylaxs
Atopy
Asthma
Allergic rhinitis
Urticaria
Angioedema
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52
Q

What are some triggers for Type 1 reaction

A

Food
Drugs
Stinging insects

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53
Q

How does IgE act in parasitic infection

A

Fab portion is bound to the worm. The Fc portion is free floating.
Eosinophils have Fc epsilon receptors that will collide with the parasite that has IgE on it and it will release Major basic proline and cause tissue damage

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54
Q

Hoe does IgE work with antigens

A

On mast cells the IgE is already docked and it waits for the antigen to bind

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55
Q

What is the mechanism of Type 2 reaction

A
  1. Ab bind to cell membrane
  2. Cellular destruction leads to activation of complement and NK killing
  3. Cellular dysfunction causes abnormal activation or blocking
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56
Q

What are some destructive examples of type 2 reactions

A 
Autoimmune hemolytic anemia
ITP
Transfusion
Hyperacute transplant rejection
Rheumatic fever
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57
Q

Classical rejection is mediated by what hypersensitivity

A

4

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58
Q

Cornelia transplant rejections are mediated by what

A

2

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59
Q

What is an example of abnormal activation in Type 2

A

Graves

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60
Q

What is an example of blocking in type 2

A

MG

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61
Q

What is Coombs serum

A

Anti human IgG

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62
Q

What does direct Coombs test look for

A

Antibodies on RBCs

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63
Q

What does indirect Coombs test look for

A

Free plasma antibodies that could bind RBC and cause lysis

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64
Q

What is the mechanism of Type 3 reaction

A
  1. Circulating Ig/GIgM complexes get lodged in vessels and tissues
  2. Complement is activated, tissue is damaged
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65
Q

What is a local manifestation of type 3 reaction

A

Arthus

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66
Q

What s arthus

A

It is a type 3 reaction
Common after vaccinations
Arm will get red

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67
Q

What are some systemic examples of type 3 reactions

A

Serum sickness
Rheumatoid arthritis
Lupus

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68
Q

What is the process of immune complexe-mediated complement activation

A
  1. Mast cell degranulation via anaphylotoxins
  2. PMN chemotacis
  3. Stimulates release of lytic enzymes from PMNs
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69
Q

Type 1,2,3 are ______ driven

A

Ab

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70
Q

Type 4 is ____ driven

A

Cell

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71
Q

Type 1 is Ig____ driven

A

E

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72
Q

Types 2-3 are Ig_ and Ig__ driven

A

G and M

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73
Q

What is the mechanism of type 4 reactions

A
  1. Antigen binds to sensitized CD4 cell
  2. CD4 releases cytokines that attract macrophages
  3. Tissue damage
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74
Q

Are antibodies involved in Type 4 reactions

A

NO

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75
Q

What are som e examples of Type 4 reactions

A

Contact dermatitis
TB test
Corneal transplant recreation
Autoimmune

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76
Q

What are the key cells in type 4 reactions

A

T helper cells

Macrophages

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77
Q

What is phlyctenular keratoconjunctivitis

A

Blisters on eye

Causes by bacteria: staphylococcus aureus

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78
Q

What is a macula

A

A flat lesion

I.e. Freckle

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79
Q

What is a patch

A

It is a bigger macule

I.e. Birthmark

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80
Q

What is a Papule

A

Elevated skin lesion

I.e mole, acne

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81
Q

What is a plaque

A

Larger than a papule

I.e psoriasis

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82
Q

That is a vesicle

A

A large fluid filled blister

I.e shingles

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83
Q

What is a bulla

A

A large fluid filled blister

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84
Q

What is a pustule

A

A vesicle filled with pus

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85
Q

What is a wheal

A

A transient smooth papule or plaque

I.e hives

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86
Q

Is lupus chronic or acute?

A

Chronic

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87
Q

Why is lupus the “great imitator?

A

It can affect virtually every organ system

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88
Q

Who does lupus affect

A

Primarily women of child bearing age

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89
Q

What s the classic triad of lupus?

A

Fever
Joint pain
Malar (butterfly) rash

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90
Q

What is lupus often misdiagnosed with

A

Arthritis

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91
Q

What is the cause of lupus

A

Unknown

But we know it Type 3, immune complex related (ANAs)

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92
Q

What is the ratio of lupus in women to men

A

10:1

Men usually get more severe

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93
Q

What are the common causes of death in lupus

A

Cardiovascular disease
Renal failure
Infections

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94
Q

What is a test you can do to look for lupus

A

ANAs
Anti-dsDNA Ab
Anti smith Ab

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95
Q

Is ANA test exclusive to Lupus

A

NO

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96
Q

What is the most common form of lupus

A

Systemic lupus erythematosis (SLE)

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97
Q

What is discoid lupus

A

Only affects the skin
(10%)
It never goes internal

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98
Q

What is drug induced lupus

A

10%

Signs/symptoms resolve upon cessation of the drug

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99
Q

What is the ANA test

A

Sensitive and not specific

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100
Q

What is the Anti-dsDNA Ab test

A

Specific, poor prognosis

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101
Q

What is the anti-Smtih Ab test

A

Specific, poor prognosis

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102
Q

What are the SLE ocular findings

A 
20% 
Dry eye
Recurrent episcleritis
Peripheral keratitis 
Photosensitivity
Uveitis  
Central retinal artery occlusion
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103
Q

What test can Lupus cause a false positive in

A

RPR/VDRL

FTA/ABS to confirm

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104
Q

What are some drugs that are associated with with drug induced lupus?

A

Quinidine
Isoniazid
Hydralazine
Procainamide

Mnemonic: Quietly Induce Harmful Pathology

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105
Q

How will the drugs that cause drug induced lupus show up in the blood

A

Transient ANA (no anti-Sm antibodies)

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106
Q

What is vasculitis

A

Inflamed vessel walls that can occlude

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107
Q

What is giant cell arteritis

A

Affects large and medium arteries

In eye and aorta

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108
Q

What is the presentation of giant cell arteritis

A

HA
Scalp necrosis
Jaw claudication
Blindess

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109
Q

What is the treatment for giant cell arteritis

A

Steroids

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110
Q

What is polyarteritis nodosum

A

Focal or segmental lesions of small and medium arteries

Causes joint pain, retinal vein occlusion, cotton wool spots

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111
Q

What is scleroderma

A

Excessive fibrosis throughout the body

Occurs in 30-35 year old women

Ususually affects the skin, but it can go in to the body and scar organs (fatal in the lungs)

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112
Q

ANA positive in _____% of patients with scleroderma

A

95

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113
Q

What is diffuse scleroderma

A

It can go to many organs of the body
Rapid progression to organs
20% 10 year survival

Pursed lips

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114
Q

What si limited scleroderma

A

Affects the skin, fingers, and face

Benign course

CREST syndrome

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115
Q

What is CREST syndrome

A

Calcinosis (calcium deposits under skin)
Raynaud phenomenon (vasospasm in digits (white-blue-red)
Esophageal Dysmotility
Sclerodactyly (thickening and tightening of skin and fingers and toes (claw fingers))
Telangiectasia (small, dilated vessels near the skin or mucus membrane surface, spider veins)

116
Q

What is the test for scleroderma (systemic)

A

ANA
Anti-Scl-70 Ab
Anti-centromere Ab

117
Q

You have a positive Anti-scale-70 Ab test, what do you have

A

Diffuse/bad scleroderma

118
Q

You have a positive anti-centromere Ab test, what do you have

A

Limited/benign scleroderma

119
Q

What are the ocular implications of scleroderma

A

May involve lacrimal glands

120
Q

What is Sjögren’s syndrome

A

Autoimmune destruction of exocrine glands

They cant spit or sweat

121
Q

What it’s eh triad of sjogrens

A

Dry mouth
Dry eyes
Arthritis

122
Q

What is the lab test for sjogrens

A

ANA/RF positive
Anti-Ro
Anti-La

123
Q

What is arthritis

A

Inflammation of the joints

124
Q

What sit eh most common cause of arthritis

A

Osteoarthritis

125
Q

What is osteoarthritis

A

Affects 27 mil in US
Involves weight bearing joints
Due to loss of cartilage
Not systemic

126
Q

What is rheumatoid arthritis

A

Systemic inflammation disease of synovial membranes and joints of hands, feet, wrists

(Also heart, lung, liver, skin, vessels)

127
Q

What is the primary mechanism of Rheutatoid arthritis

A

Starts as type 4

Goes to type 3

128
Q

What do we use to diagnosis rheumatoid arthritis

A

Rheumatoid factor
It is an autoantibody (IgM) that is specific to cartilage collagen

It is an Anti-IgG Ab
Make Ab to our own IgG

129
Q

What are the ocular manifestations of rheumatoid arthritis

A 
In 25%  of patients 
Keratoconjunctivitis sicca
Scleromalacia perforans 
Choroiditis
Retinal vasculitis
Retinal detachments
Macular edema 
Peripheral corneal ulceration
130
Q

In RA IgG causes very little activation of complement T/F?

A

True

131
Q

what is keratoconjunctivitis sicca

A

Decrease tear production

15-25%

132
Q

What is scleromalacia perforans

A

Necrotizing scleritis without inflammation

15% caused by RA

133
Q

What is juvenile idiopathic Arthritis (JIA)

A

Common in children
ANA positive
RF negative in (50%) (if present they will have a worse outcome)

134
Q

JIA is the most Mormon cause of what in children

A

Uveitis (80%)

135
Q

What are seronegative spondyloarthropathies?

A

Arthritis without RF

136
Q

What are seronergtive spondyloarthropathies associated with strongly?

A

HLA-B27 (MHC-I)

137
Q

What are the signs of Seronegative spondyloartropathies

A

Inflammation in back (worse in morning)

Uveitis
Rashes
GI symptoms
Dactylitis (sausage fingers)

PAIR
P:psoriatic arthritis 
A: ankylosis spondylitis 
I: IBD
R: Reiters syndrome
138
Q

Who is ankylosing spondylitis more common in

A

Men

139
Q

What would a radiology scan reveal in ankylosing spondylitis

A

Bamboo spine (vertebral fusion)

140
Q

What is the classic triad of reactive arthritis

A

Conjunctivitis
Urethritis
Arthritis

Can’t see, cant pee, cant climb a tree

141
Q

What is sarcoidosis

A

A non-rheumatologist autoimmune
Inflammatory disease
Associated with uveitis and hypercalcmia

142
Q

What is a common sign of sarcoidosis

A

Non-case acting granuloma skin lesions

143
Q

You do a test and find a high calcium what are you worried about?

A

Parathyroid
Sarcoidosis
Lung cancer

144
Q

What is the indicator of impetigo

A

Honey colored lesions

145
Q

What causes upetigo

A

Gram positive bacteria

146
Q

What are the 2 gram positive bacteria responsible for impetigo

A

Staph aureus

Group A beta-hemolytic streptococci

147
Q

What are the 2 types of impetigo

A

Impetigo contagiosa

Impetigo bullosa

148
Q

It impetigo contagious?

A

Yes, highly

149
Q

How does impetigo contagosa appear

A

Crusty pustules

150
Q

How does impetigo bullosa appear

A

Bulla
Honey colored
Usually called by S. Aureus

151
Q

Where does impetigo occur

A

Common sites of S. Aureus colonization (nose and face)

Secondary infections of dermatomes, breaks in skin, and wounds can occur

152
Q

What accumulates in impetigo

A

Neutrophils accumulating in stratum cornermen

Leads to subcorneal pustule that raptures and crusts

153
Q

What is the pathogenesis of blister formation

A

Bacteria produce toxin that cleaves desmoglein

154
Q

What Ecthyma (impetigo)

A

Deeper infection

Results in erosion to dermis

155
Q

What is folliculitis

A

Staphylococci infection of hair follicles

156
Q

What are the signs and symptoms of folliculitis

A

Itching and burning

157
Q

What areas can be affected with folliculitis

A

Any region with hair

Especially axilla, face, legs

158
Q

What is a faruncule

A

It occurs in the setting of staphylococcal folliculitis

Initially a firm nodule that develops an abscess, sometimes with a central pustule

159
Q

What WBC is in furuncule

A

Neutrophils

160
Q

What is a carbuncle

A

Composed of multiple, coalescing furuncules

Colin’s subcutaneous abscesses, superficial pustules
And openings draining pus

161
Q

What is erysipelas

A

A beta hemolytic strep colonize skin and spread along superficial lymphatic vessels

Erythematous expanding plaque

162
Q

What is psoriasis

A

A common infection that infects 1-2% of US

It affects all ages

163
Q

Is psoriasis itchy?

A

NO

164
Q

What is psoriasis often associated with

A

Psoriatic arthritis
Myopathy
Enteropathy
AIDS

165
Q

What areas of the body are often affected by psoriasis

A 
Elbows
Knees
Scalp
Lumbosacral
Intergluteal cleft
Glans penis
166
Q

What is the classic presentation of psoriasis

A

Well demarcated
Pink/salmon colored
Silver/white scales

167
Q

Does psoriasis affect the nail

A

Yes
In 30% of cases

Has pitting, yellow-brown discoloration

168
Q

What is histologically happening in psoriasis

A

There is an increase in epidermal cell turnover that leads to acanthosis (epidermal thickening)

169
Q

What mediates Psoriasis

A 
T cells
It has a strong association with HLA-C
CD4+T cells interact with antigen cells in skin
CD8+T cells are activated 
Cytokines released
170
Q

What is the rate of occurrence of seborrheic dermatitis

A

It is more common than psoriasis

171
Q

What is affected in seborrheic dermatitis

A

Areas with high densities of sebaceous glands

Scalp, forehead, external auditory canal, retroauricular area, nasolabial folds, presternal area

172
Q

What causes dandruff

A

Seborrheic dermatitis

173
Q

How does early seborrheic dermatitis appear

A

Similar to eczema

174
Q

How does late seborrheic dermatitis appear

A

Similar to psoriasis

175
Q

What causes follicular lipping in seborrheic dermatitis

A

Mounds of parakeratosis containing neutrophils and serum

176
Q

What causes seborrheic dermatitis

A

Unknown

177
Q

How does lichen planus classically appear

A

Pruritic, purple, polygonal papules

Often highlighted by Wickham striae

178
Q

When does lichen planus clear?

A

Spontaneously after 1-2 years

Can leave behind hyperpigmentation

May progress into malignancy

179
Q

What is pemphigus

A

A rare, autoimmune blistering disorder that usually affects people older than 40

180
Q

What is the most common variant of pemphigus

A

Pemphigus vulgaris

181
Q

How does pemphigus vulgaris occur

A

Involves mucosa and skin (scalp, face, axilla, groin, trunk, other pressure points)

182
Q

How does pemphigus vulgaris appear

A

As superficial vesicles and bull are that rupture easily

Dried serum, crust

183
Q

What is in the sera of pemphigus vulgaris

How are they deposited

A

IgG Ab to desmogleins

In a fish net pattern

184
Q

Who is affected by bullous pemphigoid

A

Elderly

185
Q

How does bullous pemphigoid appear

A

Tense bullae filled with clear fluid
They do NOT rupture easily
Heal without scarring

186
Q

What areas are affected by bullous pemphigoid

A 
Inner thighs
Flexor surfaces of forearms
Axilla
Groin
Lower abdomen 
Oral lesions (30%)
187
Q

Is bullous pemphigoid acantholytic

A

No

188
Q

What antigen causes bullous pemphigoid

A

Antigens in hemidesmosomes

189
Q

What is acne vulgaris

A

Adolescent acne
It is a disorder of sebaceous follicles

Hereditary

190
Q

What causes acne vulgaris

A

Androgenic hormones cause abnormal keratinization of follicles
Sebaceous ducts are blocked
Comedone

191
Q

What bacteria causes acne

A

Propionibacterium acnes

192
Q

How does bacteria cause acne

A

Bacterial lipases convert lipids to sebum to pro-inflammatory fatty acids

193
Q

How does mild acne appear

A

Comedones

Occasional papules and pustules

194
Q

How does moderate acne appear

A

More inflammatory

Lesions may heal with scars

195
Q

How does cystic acne appear

A

Learner, deeper, more numerous papules or pustules
Lesions tend to occur on trunk
Not true cysts

196
Q

What does trunk involvement indicate in acne

A

That treatment will be difficult

197
Q

How does healing occur in severe acne

A

Atrophic or pitted scars on face
Hypertrophic scars or keloids on back

Hyperpigmentation

198
Q

What is Rosacea commonly mistaken for

A

Acne

199
Q

How does acne differ from rosacea

A

Rosacea does not have comedones

Lesions are usually on flush areas, nose, cheeks, forehead, chin

200
Q

What causes rosacea

A

Idiopathic

No inherited patterns

201
Q

Does rosacea have ocular involvement

A

Blepharoconjunctivitis

202
Q

What are the precipitating factors for rosacea

A

Sun exposure
Excessive face washing
Irritating cosmetics

203
Q

What is rhinophyma

A

Disfiguring sebaceous hyperplasia

It is an enlarged red nose

204
Q

How does pre-rosacea appear

A

Facial erythema and telangiectasias “rosy cheek”

Most patients never develop inflammatory lesions

205
Q

What is vitiligo?

A

Loss of melanocytes in affected skin

206
Q

What makes vitiligo more prominent

A

Tanning of surrounding areas

207
Q

What can cause the loss of pigmentation in vitiligo

A

Infection
Dermatitis
Chemical irritation
Idiopathic

208
Q

What is melasma

A

Enhanced pigment transfer from melanocytes

209
Q

What is melasma associated with

A

Pregnancy

Oral contraceptives

210
Q

What accentuates melasma

A

Sun exposure

It resolves spontaneously or after hormone administration is discontinued

211
Q

What is lentigines

A

Localized hyperplasia of melanocytes
Birthmark
Common in infancy or childhood

212
Q

How does lentigines appear

A

Oval, tan-brown macules or patches

Cafe au lait spots

213
Q

How does lentigo differ from freckles

A

Lentigo does not darken in sunlight

214
Q

What can too many cafe au lait spots be indicative of

A

Neurofibromatosis type I

215
Q

What is solar lentigines

A

Develop with age and sun exposure “liver spots”

216
Q

What causes scabies

A

Sarcoptes scabei

217
Q

How is scabies spread

A

Person to person

Fomites

218
Q

Where are mites typically found

A

Between fingers and on wrists

219
Q

Where are the common locations of scabies rash to occur

A

Buttocks, back, lumbar, elbows, armpits, groin, knees, umbillicus , hands, heel

220
Q

What is the pathognomonic lesion of scabies

A

Burrow

221
Q

How do burrows form in scabies

A

Adult female burrows and deposits eggs
The egg hatches
Larvae molt into nymphs (found in molting pouches)
Male will penetrate molting pouch and mating

222
Q

What are nevocellular nevi?

A

Moles
Congenital or acquired

Tan/brown, with unform papules and borders

223
Q

What are nevocellular nevi formed from

A

Melanocytes that have become round

Occurs at tips of rete ridges

224
Q

What are junctional nevi

A

Flat

Can grow into dermis and form compound nevi

225
Q

What is a compound nevi

A

Have cords of nevus cells in dermis

Raised, dome shaped

Have matured (produce no melanin)

226
Q

What is sporadic dysplastic Nevi

A

Malignant

Transformation is rare

227
Q

What is familial dysplastic nevi

A

Precursors of malignant melanoma
Heritable
Lifetime risk of maligned degeneration is 100%

228
Q

How does dysplastic nevi differ from nevi

A

Larger than acquired nevi
Can occur as hundreds of lesions
Any body surface is prone, no just sun exposed regions
Coloration not constant

229
Q

What is dysplastic nevi

A

Compound nevi with abnormal growth

Nevus cells are enlarged and fused
Hyperchromasia (parallel bands of fibrosis)

230
Q

What is the clinical presentation of acanthosis Nigricans

A

Thickened hyperpigmented skin
Sometimes skin tags
Occurs in armpit, neck, groin, anogenital

231
Q

What is acanthosis nigricans an important marker for

A

Malignant conditions

80% benign (obesity/insulin dependents, endocrine, drug admin)

Malignant (tumors produce factors that promote epidermal growth)

232
Q

What is the clinical presentation of keratoacanthoma

A

Single lesion
Grows rapidly (3-4 was)
Ulcer forms a lesion center (crater) center has keratin mass

Sunexposed skin(face, ears, back of hands and arms)

Resolves in 3-4wks with an irregular scar

Can progress in to squamous cell carcinoma (may be removed)

233
Q

What is the clinical presentation of seborrheic keratosis

A

After 3040 yo
Trunk, shoulder, face, scalp

Begin small, yellow/tan plaque that increases in thickness and developers a greasy crust

Black or brown with sharp demarcation

Verruous surface

May be removed

234
Q

What should you be aware of in seborrheic keratosis

A

Development of multiple legions

Can be a sign of Leser-Trelat (malignancy)

235
Q

What is the clinical presentation of actinic keratosis

A

Occurs on exposed fair older skin
Chronic UV exposure
Ill defined erythematous macules or papules with a scaly surface

Premalignant (can progress to squamous cell carcinoma in not treated)

236
Q

What can actinic keratosis be a source of

A

Cutaneous horns

237
Q

What is the clinical presentation of squamous cell carcinoma

A

Red/scaling plaques
Nodular, tan hyperkeratotic lesions that can ulcerate

Oder (60y.o)

238
Q

What are the risk factors for squamous cell carcinoma

A 
Sun exposure
Fair complexion
Carcinogens
Old burns
Arsenic ingestion
Chronic ulcers and draining osteomyelitis
Chewing tobacco (oral)
Xeroderma pigmentosa
239
Q

When is squamous cell carcinoma usually discovered

A

When small and respectable (5% metastasized)

240
Q

What can be associated with squamous cell carcinoma

A

Cutaneous horns

Leukoplakia when oral mucosa is involved

241
Q

SCC

Squamous epithelium extends beyond basement membrane into dermis

In ALL layers of epidermis

A

Know this

242
Q

What is the clinical presentation of basal cell carcinoma (BCC)

A 
Common
Slow growing
Aggressive 
Pearly papules with telangiectasias 
Occurs in sun exposed, hair bearing areas

Rare to metastasize

243
Q

What is rodent ulcer in reference to BCC

A

When it loses its distinct border but continues to grow across the skin

244
Q

What are the risk factors for BCC

A

Chronic sun exposure
Fair complexion
Immunosuppression
Xeroderma pigmentosum

245
Q

What is the clinical presentation of malignant melanoma

A

40-70
Males: upper back
Females: back and legs

Asymptomatic (can itch)

Usually >1cm

246
Q

What are in the important clinical signs of malignant melanoma

A

Asymmetry
Border irregularity
Color
Diameter >1cm

247
Q

What are the risk factors for malignant melanoma

A

Intermittent sun exposure
Bad sunburns in past
Fair skin
Dysplastic nevus syndrome (50% at age 60)

248
Q

What re prognostic indicators of malignant melanoma

A

Depth of invasion

Tumors that have horizontal growth have best prognosis

Vertical growth: BAD

249
Q

What are some horizontal growth patterns of malignant melanoma

A

Lentigo malignant melanoma

Superficial spreading melanoma

Acral -lentiginous melanoma

250
Q

Lentigo maligna melanoma

A

Usually on face or neck

Best prognosis

251
Q

Superficial spreading melanoma

A

Most common for Caucasians

Stays in situ for months

252
Q

Acral lentiginous melanoma

A

Most common in dark skin

Hands, feet, subungal area

253
Q

What melanoma growth has the worst prognosis

A

Vertical growth

254
Q

Tumor growth <0.76 mm vertical tells you that…..

A

Metastasis is unlikely

255
Q

What is the cause of carotid stenosis

A

Build up of atherosclerotic plaque in the lumen of the common carotid near the bifurcation

256
Q

What effect does stenosis have on vessels

A

Reduces blood flow (Can be symptomatic if mild)

Can lead to thrombosis at stenotic site or formation of emboli which occlude major arteries

Drop in BP

257
Q

What are the major arteries that can be affected by Carotid stenosis

A

Middle cerebral artery *
Anterior cerebral artery
Ophthalmic Artery

258
Q

What s amaurosis fugax?

A

Transient/acute monocular blindness

259
Q

What can be found in a physical exam that is associated with carotid stenosis

A

Bruit

260
Q

How do you define the severity of carotid stenosis

A

By the degree of narrowing of the lumen

261
Q

What is carotid endarterectomy?

A

Surgical removal of the atherosclerotic buildup

High risk

262
Q

What are some alternative treatments for patients with carotid stenosis if carotid endarterectomy is too risky

A

Angioplasty

Stenting

263
Q

What can patients with carotid stenosis develop

A

Carotid occlusion

264
Q

What is carotid occlusion

A

Complete filling collusion of a long segment of the internal carotid
They are functionally intact due to compensation through collateral blood flow via circle of Willis

Thrombi can form at distal end of occlusion (endarterectomy too risky)

265
Q

What is a carotid/vertebral dissection?

A

Trauma-induced tear in the inner lining of a vessel

Creates a flap of tissue in the lumen that can occlude the vessel

266
Q

T/F the patient could hear popping at time of tear in dissection

A

True

267
Q

What is the complication what can occur with carotid/vertebral dissection

A

Thrombosis along the dissection flap and then occlusion occurs

268
Q

What is the presentation of carotid/vertebral occlusion

A

Pain in distribution areas
Transient ischemic attack signs
Infarct
Horners syndrome ipsilaterally

269
Q

What is vasculitis

A

Inflammatory disease in large arteries (elastic lamina)

Can lead to ischemia distal to origin site

270
Q

What arteries can be involved in vasculitis

A

Superficial temporal
Vertebral
Ophthalmic
Posterior ciliary (Small)

Extramural arteries

271
Q

What is temporal arteritis

A

Risk of secondary ischemia due to occlusion or significant narrowing

Ischemia in CNS

Transient of ongoing visual loss

272
Q

Is temporal arteritis an emergency?

A

YES
They can develop blindness

Treat with glucocorticoids

273
Q

What is the presentation of temporal arteritis

A

Visible blood loss perfusion in affected side of face

Fever, ache, pain, scalp tenderness, HA
Jaw claudication
Weight loss
Anemia
Can be associated with peripheral neuropathies 
White swelling around the optic disc
274
Q

Who gets temporal arteritis

A

Rare under 50
Common over 70
Women
White peoples

275
Q

How o you disgnose temporal arteritis

A

Biopsy of temporal artery

Angiogram

276
Q

What is Graves’ disease

A

Autoimmune

Common origin for orbital disorder in adults

277
Q

What causes Graves’ disease

A

Ab target TSH receptors,
Increase T3/4
Can produce toxicity to thyroid tissue

278
Q

What causes orbital signs in Graves’ disease

A

Lymphocytic infiltration

279
Q

What is the presentation of hyperthyroid disease

A

Goiter
Tachycardia
Fatigue, weight loss, anxiety, heat intolerance, sweating, increased appetite

280
Q

What are the orbital signs associated with graves

A 
Periocular swelling
Lid retraction
Bulging eyes
Diplopia
Disconjugate gaze
Oculomotor deficits 
Foreign body sensation 
Pain during eye movements
281
Q

What is craniopharyngeal carcinoma

A

Invades intracranial if it spreads to cranial sinuses

282
Q

What is nasopharyngeal carcinoma

A

Invade intracranially if it spreads to the sinuses

283
Q

What is laryngeal carcinoma

A

Common in smokers, presents with hoarseness
Cervical lymphadenopathy

Less likely to invade CNS

284
Q

What is salivary carcinoma

A

Common form from parotid gland
Can invade toward CNS along facial nerve

Less likely to invade to lead to visual oculomotor system disturbances

285
Q

What is lymphoma

A

CNS essential lacks lymphatic vessels and nodes

Primary CNS lymphoma (rare from glial cells)
Chronic: in lymph vessels /nodes. Benign

Pathology (4 decks)

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